Very interesting! I know for myself (no celiac, no *diagnosed* IBS) that standard wheat causes bloating, cramping and constipation (and allergies). I know that I can eat spelt, and sprouted grains to some extent.

I saw einkorn past at the Food Coop and considered trying it.

Interesting. Thanks.

I can vouch for that.
I'm wheat intolerant but I can eat durum and rye without reacting.
I haven't tried spelt flour yet as I can't have yeast so bread as a test is out.

Those are the only three that I'm aware of that are considered to be ancient wheats.

New info coming out at the Digestive Disease Week 2014 meetings this week (quote on Medscape from Dr David Johnson, Professor of Medicine, Chief of Gastroenterology at Eastern Virginia Medical School in Norfolk, Virginia). Lectures from American Gastroenterological Association and the American Society for Gastrointestinal Endoscopy:

quote: "Then we get into the whole area of irritable bowel syndrome, microflora, dietary manipulations, and the FODMAP diet. A double-blind, randomized controlled trial[6] on a low-FODMAP diet compared with a gluten-free diet is going to be presented. It will be followed by Lin Chang's summary[7] of where we are with these dietary manipulations.

The next topic really caught my attention because it is a specific area of interest for me. This is a human gut microbial cluster analysis looking at potential brain-gut signatures.[8] They actually found a microflora cluster that they could identify with a brain-gut signature. This pilot study is very provocative. There is antigen processing in the gut. It is the largest immunologic processing system in our body, and changes in the microflora may have profound influences on disease." unquote

** 6.Piacentino D, Rossi S, Alvino V, et al. Effects of Low-FODMAP and gluten-free diets in irritable bowel syndrome patients. a double-blind randomized controlled clinical study. Program and abstracts of Digestive Disease Week; May 3-6, 2014; Chicago, Illinois. Abstract 374.

** 7.Chang L. IBS and FODMAP. Program and abstracts of Digestive Disease Week; May 3-6, 2014; Chicago, Illinois. Abstract Sp463.

** 8.Labus JS, Mayer EA, Derrien M, et al. Human gut microbial clusters correlate with anatomical brain signatures: a pilot study. Program and abstracts of Digestive Disease Week; May 3-6, 2014; Chicago, Illinois. Abstract 375.

quote: "The last presentation that really caught my eye is a multicenter trial.[18] This is a new first-in-class drug, larazotide acetate, which is an oral peptide that regulates tight junctions. A patient with celiac disease might have some real advantage. As you know, celiac disease is problematic due to inadvertent exposure and noncompliance. Every time this happens, there is a change in the tight junctions, which controls the paracellular permeability and upregulation of inflammatory mediators and cytokines. This is an oral peptide that regulates the tight junctions. This study looked at 74 centers in the United States with 342 patients and has very interesting data. I won't share with you the final results, but they look very promising and represent a new approach to a problematic disease that affects about 1% of people in the United States alone." unquote

** 18.Wang C, Rasmussen H, Perrow W, et al. Larazotide acetate, a first in-class, novel tight junction regulator, meets primary endpoint and significantly reduces signs and symptoms of celiac disease in patients on a gluten-free diet: results of a multicenter, randomized, placebo controlled trial. Program and abstracts of Digestive Disease Week; May 3-6, 2014; Chicago, Illinois. Abstract 929f.

Liana

More from the Digestive Disease Week 2014 sessions in Chicago this past week. (www.ddw.org)


Prevalence of Fructose Malabsorption in Patients With Irritable Bowel Syndrome After Excluding Small Intestinal Bacterial Overgrowth

Sa1179 |
Kee Wook Jung1, Young Hwan Cho1, Young-Ok Park2, So Yoon Yoon2, JungBok Lee3, Jong Wook Kim1, Dong-Hoon Yang1, In Ja Yoon1, So Young Seo1, Hyo Jeong Lee1, Sang Hyoung Park1, Kyung-Jo Kim1, Byong Duk Ye1, Jeong-Sik Byeon1, Hwoon-Yong Jung1, Suk-Kyun Yang1, Jin-Ho Kim1, Seung-Jae Myung1


Print Affiliation
1Gastroenterology and Hepatology, Asan Medical Center, Seoul, Republic of Korea; 2Clinical Nutrition, Asan Medical Center, Seoul, Republic of Korea; 3Clinical Epidemiology and Biostatistics, Asan Medical Center, Seoul, Republic of Korea

Abstract:

BACKGROUND: Fructose malabsorption (FM) mimics the symptoms of irritable bowel syndrome (IBS), and its prevalence has rapidly increased because of the frequent use of fructose in food products. However, diagnosing FM in IBS is challenging because of its overlap with small intestinal bacterial overgrowth (SIBO) and the differences among fructose dosage cutoffs that distinguish between FM and normalcy, especially in Asian individuals, in hydrogen breath testing (HBT). We assessed the prevalence of FM by comparing patients with IBS with asymptomatic control individuals after excluding SIBO using the glucose HBT. We also evaluated the effective fructose dosage for HBT. In addition, we assessed the differences between the dietary habits of patients with IBS and asymptomatic control individuals.
METHODS: From December 2011 until November 2012, patients with IBS were identified using the ROME III questionnaire, and the asymptomatic control individuals were prospectively enrolled in the study. Dietary habits were determined using the Food Frequency Questionnaire (FFQ) and responses were analyzed using a computer-aided nutritional (CAN) analysis program. After excluding SIBO using the 75-g glucose HBT, the enrolled participants were tested using both the 15- and 25-g fructose HBTs, with an interval of at least 1 week.
RESULTS: After excluding SIBO-positive patients and those that dropped out of the study during follow-up (n=18), 35 patients with IBS (male:female [M:F] ratio=16:19, mean age= 43 ± 14 years) and 35 asymptomatic control individuals (M:F ratio = 18:17, mean age = 38 ± 11 years) were enrolled in the study. The 15-g fructose HBT yielded positive results in seven of the 35 (20.0%) patients with IBS and in two of 35 (5.7%) asymptomatic control individuals (P = 0.07). The 25-g fructose HBT yielded positive results in 16 of the 35 (45.7%) patients with IBS and in eight of the 35 (22.9%) asymptomatic control individuals (P = 0.04). CAN analysis of the FFQ responses showed no significant differences between the two groups in relation to total calorie intakes, and protein, lipid, carbohydrate, and fructose consumption. However, patients with IBS showed a significantly higher mean fiber intake than that of the control individuals (21.24 ± 11.35 g in patients with IBS vs. 15.87 ± 7.07 g in asymptomatic control individuals, P = 0.04).
CONCLUSIONS: Use of the 25-g fructose HBT enabled identification of FM in a significantly higher percentage of SIBO-negative patients with IBS than in asymptomatic control individuals, suggesting that FM is closely correlated with IBS. Education regarding dietary control of foods containing fructose may be useful for the management of patients with IBS.

Disclosure(s):
The following people have nothing to disclose: Kee Wook Jung, Young Hwan Cho, Young-Ok Park, So Yoon Yoon, JungBok Lee, Jong Wook Kim, Dong-Hoon Yang, In Ja Yoon, So Young Seo, Hyo Jeong Lee, Sang Hyoung Park, Kyung-Jo Kim, Byong Duk Ye, Jeong-Sik Byeon, Hwoon-Yong Jung, Suk-Kyun Yang, Jin-Ho Kim, Seung-Jae Myung





Non Celiac Gluten Sensitivity (NCGS) Is Outnumbered by FODMAPS Sensitivity in Patients Spontaneously Adhering to Gluten Free Diet (GFD): a Two Stage Double Blind Prospective Study

Sa1989 |
Barbara Zanini, Monica Marullo, Chiara Ricci, Francesco Lanzarotto, Alberto Lanzini


Print Affiliation
Scienze Cliniche e Sperimentali-Gastroenterology Unit, University of Brescia, Brescia, Italy

Abstract:

Adverse gastrointestinal and extra intestinal reaction to gluten containing food is reported by many patients that spontaneously adhere to GFD without medical necessity because of exclusion of celiac disease (CD). It is unknown how many of these patients fulfil the criteria for NCGS, a still poorly defined clinical entity of uncertain pathogenesis, and whether cereal components other than gluten may cause symptoms.
Our aim was to assess gluten dependence of symptoms in patients spontaneously adhering to GFD for self diagnosed adverse reaction to gluten containing diet.
Patients spontaneously adherent to GFD without medical necessity referred to our Clinic in years 2008-2011 were recalled and randomized to a double blind cross over study involving, while continuing GFD, daily administration of 10 g gluten Vs 10 g gluten free flour for 10 days each with 2 weeks wash-out in between (challenge stage). Patients were subsequently instructed to keep on a low FODMAPs diet for 8 weeks (low FODMAPs stage) Endpoints: ability to clearly identify the gluten phase of the challenge stage, and changes of Gastrointestinal Symptoms Rating Scale (GSRS) and of visual analogue fatigue scale, changes of antigliadin (AGA) IgA/lgG and anti tissue transglutaminase (t-TG) IgA between baseline and various steps of the two stages of the study.
Out of 86 patients recalled 45 persisting on GFD fulfilled exclusion criteria for CD. 25 patients (age 42 + 9 years, M/F = 2/23, 10 HLA DQ2/8 positive, 13 negative, 2 unknown) signed the informed consent and were randomized. During the challenge stage the gluten phase of the study was correctly, incorrectly, or not clearly identified by 8, 12 and 5 patients, respectively. In the 8 gluten sensitive patients recognizing the gluten phase (4 with HLA DQ2/8), scores for the 3 dimensions of GSRS (pain, indigestion and diarrhoea), but not those for fatigue scale, were higher during the gluten compared with the no gluten phase (figure 1) and with baseline values (not shown). Scores in the 12 patients not recognizing the gluten phase were worse during the gluten free flour phase than during the gluten phase. No change in transglutaminase antibody level was observed at any time point. During the low FODMAPs stage of the study there was a trend for the 5 dimensions of the GSRS to be reduced in the gluten sensitive patients, and the score of indigestion dimension (borborygmus, bloating, eructation, flatus) was significantly reduced in patients incorrectly identifying gluten (FODMAPs sensitive, figure 2) and with worsening of symptoms during the gluten free flour phase of challenge.
The population of patients reporting intolerance to gluten containing food is a mixed population of gluten sensitive (NCGS) and of FODMAPs sensitive patients. NCGS is uncommon and is outnumbered by FODMAPs sensitivity in patients spontaneously adhering to GFD.

(There were charts/graphs/ here I could not copy to this forum - Liana)

Disclosure(s):
The following people have nothing to disclose: Barbara Zanini, Monica Marullo, Chiara Ricci, Francesco Lanzarotto, Alberto Lanzini




Larazotide Acetate, a First in-Class, Novel Tight Junction Regulator, Meets Primary Endpoint and Significantly Reduces Signs and Symptoms of Celiac Disease in Patients on a Gluten-Free Diet: Results of a Multicenter, Randomized, Placebo Controlled Trial

11:00 | 929f |
Chao Wang1, Henrik Rasmussen1, Wendy Perrow1, Ciaran P. Kelly2, Daniel Leffler2, Peter Green3, Richard N. Fedorak4, Anthony J. DiMarino5, Premysl Bercik6, Joseph A. Murray7, Natalie M. Bachir8


Print Affiliation
1Alba Therapeutics, Baltimore, MD; 2Harvard Medical School, Boston, MA; 3Columbia University, New York, NY; 4University of Alberta, Edmonton, AB, Canada; 5Thomas Jefferson University Hospital, Philadelphia, PA; 6McMaster University, Hamilton, ON, Canada; 7Mayo Clinic, Rochester, MN; 8Essentia Health Duluth Clinic, Duluth, MN

Abstract:

Background: Celiac disease (CeD) is a genetic autoimmune condition affecting 1% of the western population. Triggered by the ingestion of gluten, CeD is managed by a Gluten-Free diet (GFD), however recurrent symptoms due to inadvertent exposure and non-adherence to GFD are common and found in up to 71.8% of individuals with CeD. Symptoms can significantly impact quality of life and the disease is associated with an increased risk of gastrointestinal (GI) cancers and T-cell lymphoma. Tight junctions (TJ) control paracellular permeability, increased in CeD, caused in part, by an inflammatory immune response subsequent to paracellular transport of gluten peptides into the intestinal lamina propria through epithelial TJs. Larazotide acetate is a first-in-class oral peptide that prevents TJ opening and reduces gluten uptake, inhibiting gluten and cytokine-induced intestinal permeability and inflammation in vivo. The aim of the study was to investigate the efficacy of Larazotide acetate to improve signs and symptoms in individuals with CeD while on a GFD.
Methods: In this outpatient, randomized, parallel, double-blind, placebo-controlled, multicenter study, conducted in 74 sites in North America, 342 CeD patients on a GFD for ≥12 months were randomized to receive placebo or Larazotide acetate 0.5, 1, or 2 mg three times daily (TID). The 20-week study had a 4-week placebo run-in, 12-week treatment phase, and 4-week placebo run-out. The primary outcome was the average on-treatment score in the Celiac Disease Gastrointestinal Symptom Rating Scale (CeD GSRS) domains of Diarrhea, Indigestion, and Abdominal pain.
Results: The primary endpoint of symptom reduction was met at the 0.5 mg dose of Larazotide acetate compared with placebo in both Modified Intention To Treat (MITT) (ANCOVA p=0.022, MMRM p=0.005) and Per Protocol (PP) analysis (ANCOVA p=0.007, MMRM p=0.001) (Figure 1). The 0.5 mg dose showed favorable outcomes for CeD Patient Reported Outcome (CeD PRO) GI domain, decrease in CeD PRO Symptomatic days (MITT ANCOVA 0.017) (Figure 2), an increase in Symptom-Free days (MITT ANCOVA p=0.034) and a decrease in Non-GI symptoms (MITT ANCOVA p=0.010). No increases in anti-tTG (IgA and IgG) titers were observed at any dose of Larazotide acetate. Safety of Larazotide acetate was comparable to placebo.
Conclusion: Larazotide acetate 0.5 mg reduced GI and non-GI symptoms, while reducing the number of Symptomatic days. The safety and tolerability profile of Larazotide acetate was comparable to placebo. This study represents the first large therapeutic trial in CeD to meet its primary endpoint of reducing signs and symptoms and is the first successful trial of a novel class of agents targeting TJ regulation. Larazotide acetate 0.5 mg has the potential to be the first pharmacologic CeD treatment and warrants further investigation in Phase III clinical trials.


Disclosure(s):
Wendy Perrow - Employment: Alba Therapeutics
Ciaran P. Kelly - Advisory Committees or Review Panels: Alba Therapeutics, Alvine, Merck & Co, Regeneron, Glaxo Smith Kline, Optimer, Sanofi-Pasteur, ImmunoSanT, Cubist; Consulting: CSL Behring, CSL Behring
Daniel Leffler - Consulting: Alba, Alvine, Shire, Ironwood
Peter Green - Board Membership: alvine pharmaceuticals
Richard N. Fedorak - Advisory Committees or Review Panels: Abbvie, Aptalis Pharma, Ferring Pharmaceuticals, UCB Pharma, Shire Pharmaceuticals Group, Procter & Gamble Pharmaceuticals , VSL3 Inc, Pfizer Inc , Janssen-Cilag, Merck Inc, Celtrion; Grant/Research Support: Canadian Institutes of Health Research; Stock Shareholder: Metabolomic Technologies Inc
Premysl Bercik - Advisory Committees or Review Panels: Janssen Canada, Forest Laboratories; Grant/Research Support: Nestle, Switzerland
Joseph A. Murray - Advisory Committees or Review Panels: Alvine, Enteromedics, flamentera; Consulting: Ironwood Pharmaceuticals Inc., Vysera, Iralnd, Torax Medical , AMAG, Enterohealth, Bioline Rx, GSK
The following people have nothing to disclose: Chao Wang, Henrik Rasmussen, Anthony J. DiMarino, Natalie M. Bachir




Obviously, the teams involved in the drug trial have been members of panels for drug companies, just FYI. Take it for what it's worth.

You can probably find out more from your MD or gastroenterologist. print this info out & give it to them so they can do some research for you.

Hmm, those studies are very interesting. I'm a little suprised the drug trial was looking for reduction of symptoms and signs rather than reduction of the body's reaction to gluten. In my mind, there's no use having a pill that makes eating gluten feel as good as eating something else if the villi still die in the long run - otherwise, you just post-pone the inevitable issues with malnutrition.

I'm interested to see what further studies are done in this direction, and hopefully they'll be done with less drug-company connections - or at least repeated often enough by other researchers to validate results.

Yes, it was unclear if the symptom decrease was due to less permeability of the intestine (ie healthier villi) or just damping down general body response to the leaking proteins...